eMedicine Specialties > Pulmonology > Occupational Lung Diseases

Farmer's Lung

Author: Laurianne G Wild, MD, FAAAAI, Acting Chief and Associate Professor of Clinical Medicine, Section of Clinical Immunology, Allergy and Rheumatology, Director, Allergy and Clinical Immunology Fellowship Training Program, Tulane University Health Sciences Center; Director, Allergy and Immunology Clinic, Veteran's Administration Medical Center at New Orleans
Coauthor(s): Eduardo E Chang, MD, Fellow, Department of Allergy and Immunology, Tulane University
Contributor Information and Disclosures

Updated: Apr 16, 2009

Introduction

Background

Farmer's lung is a type of hypersensitivity pneumonitis. Hypersensitivity pneumonitis, also known as extrinsic allergic alveolitis, is an immunologically mediated inflammatory disease of the lung involving the terminal airways. The condition is associated with intense or repeated exposure to inhaled biologic dusts. The classic presentation of farmer's lung results from inhalational exposure to thermophilic Actinomyces species and occasionally from exposure to various Aspergillus species.

The effect of these antigens in farmers was described as early as 1713. In Britain in 1932, Campbell described a disorder of the lung caused by inhalation of dust from moldy hay. In 1964, Ramazzini and Wright1 described workers getting "diseases of the chest."

Thermophilic actinomycetes species include Saccharopolyspora rectivirgula (formerly Micropolyspora faeni), Thermoactinomyces vulgaris, Thermoactinomyces viridis, and Thermoactinomyces sacchari, among others. These organisms flourish in areas of high humidity and prefer temperatures of 40-60°C.

The thermophilic actinomycetes are ubiquitous organisms usually found in contaminated ventilation systems and in decaying compost, hay, and sugar cane (bagasse). Exposure to large quantities of contaminated hay is the most common source of inhalational exposure for farmers who develop farmer's lung; therefore, grain farmers are not at risk for the development of the disease. Farmer's lung is often a disease of dairy farmers who handle contaminated hay during the winter months. Most cases of farmer's lung occur in cold, damp climates in late winter and early spring when farmers use stored hay to feed their livestock.

Exposure to the causative antigens depends on the type of farming, industry, and climate in the area. Note that farming practices are changing with time and that new antigens may be introduced or disappear from a region (eg, the disappearance of bagassosis in Louisiana sugar cane workers,2 the appearance of Pseudomonas fluorescens in machine operator's lung). The dynamic nature of this disease and the changing environment may lead to new challenges for the clinician.

In addition to the inhalational exposure to the organic dusts responsible for the hypersensitivity reaction in farmer's lung disease, allergens, chemicals, toxic gases, and infectious agents must also be considered as potential triggers of airway symptoms in symptomatic farmers. Farming is currently ranked as one of the top 3 most hazardous occupations, along with construction and mining.

Pathophysiology

The pathogenesis of farmer's lung depends on the intensity, frequency, and duration of exposure and on host response to the causative antigen. Both humoral and cell-mediated immune responses seem to play a role in pathogenesis. During acute episodes, acute neutrophilic infiltration is followed by lymphocytic infiltration of the airways. Levels of interleukins 1 and 8 and tumor necrosis factor-alpha are increased.3 These cytokines have proinflammatory and chemotactic properties. They cause the recruitment of additional inflammatory mediators, resulting in direct cellular damage and changes in the complement pathway, which provide the necessary stimuli to increase vascular permeability and migration of leukocytes to the lung.

If the acute exposure is large, a dramatic increase in inflammation leads to increased vascular permeability, which can alter the alveolar capillary units, thus promoting hypoxemia and decreased lung compliance. If the exposure is prolonged and continuous, collagen deposition and destruction of the lung parenchyma occur with resultant decreased lung volumes.

Strong evidence suggests the involvement of immune complex–induced tissue injury (type III hypersensitivity). The timing of development of symptoms after exposure supports this conclusion. The presence of antigen-specific immunoglobulin and complement activation and deposition in the lung also supports immune-complex or type III hypersensitivity in the pathogenesis of farmer's lung.

Cell-mediated, delayed-type hypersensitivity (type IV hypersensitivity) also plays a major role in the pathogenesis of this syndrome. The presence of lymphocytes, macrophages, and granulomas in the alveolar spaces and the interstitium supports this conclusion.

Frequency

United States

Farmer's lung is one of the most frequent types of hypersensitivity pneumonitis.

  • Incidence is highly variable and depends on multiple factors, such as intensity, frequency, and duration of exposure, type of farming, and climate.
  • An incidence of 8-540 cases per 100,000 persons per year for farmers has been reported.
  • Hypersensitivity pneumonitis affects 0.4-7% of the farming population.
  • In a 2007 study in the United States, farmer's lung accounted for 11% of cases of hypersensitivity pneumonitis.4

International

The prevalence of farmer's lung in the United Kingdom has been reported to be 420-3000 cases per 100,000 at-risk persons.

  • Epidemiologic surveys in France5 and Sweden6 show a cumulative prevalence of the disease in the range of 2.5-153 cases per 1000 farmers.
  • Incidence of farmer's lung in Finland is 0.7%. This figure is calculated from death certificates.7
  • As reported in 2006, farmer's lung appears to be on the decline, at least in some parts of the world. Specifically, the incidence of farmer's lung in Ireland declined from 1997-2002.8 Effective changes in farming practice and an increase in awareness of the disease has contributed to this decline.

Mortality/Morbidity

The mortality rate from farmer's lung is reportedly 0-20%.

  • Death usually occurs 5 years after diagnosis.
  • Several factors have been shown to increase mortality rates in farmer's lung, including clinical symptoms occurring more than 1 year before diagnosis, symptomatic recurrence, and pulmonary fibrosis at the time of diagnosis.
  • Comorbid factors: Although a history of smoking appears to decrease the overall risk for the development of hypersensitivity pneumonitis, a smoking history is the strongest predictor of increased respiratory symptoms once the diagnosis is made. Preexisting bronchial hyperreactivity with airway obstruction is also a factor.

Clinical

History

The clinical syndrome of farmer's lung, as with other types of hypersensitivity pneumonitis, is categorized as acute, subacute, or chronic.

  • Acute farmer's lung
    • Acute farmer's lung develops after large exposure to moldy hay or contaminated compost. Symptoms often spontaneously resolve within 12 hours to days if antigen exposure is eliminated or avoided.
    • Acute farmer's lung manifests as new onset of fever, chills, nonproductive cough, chest tightness, dyspnea, headache, and malaise.
    • If the inhalational exposure is large, patients may develop acute respiratory failure.
  • Subacute farmer's lung
    • Subacute farmer's lung manifests as chronic cough, dyspnea, anorexia, and weight loss.
    • Subacute disease is insidious in onset and may occur over weeks to months.
  • Chronic farmer's lung
    • Chronic farmer's lung results from prolonged and continuous exposure to the antigen.
    • Patients may have irreversible lung damage.
    • Patients may experience severe dyspnea at rest or with exertion.

Physical

  • Acute farmer's lung
    • Fever
    • Tachycardia
    • Nonproductive cough
    • Rales
    • Rales that persist after fever subsides
    • Wheezing (rare)
  • Subacute farmer's lung
    • Normal examination findings between presentations
    • Anorexia
    • Weight loss
    • Chronic nonproductive cough
    • Generalized fatigue
  • Chronic farmer's lung
    • Bibasilar rales
    • Clubbing - More often observed in patients with chronic farmer's lung with long-standing hypoxemia and parenchymal damage
    • Anorexia
    • More severe dyspnea
    • Weight loss
    • Impaired exercise tolerance

Causes

  • Thermophilic actinomycetes
    • S rectivirgula (formerly M faeni)
    • T vulgaris
    • T viridis
    • T sacchari
    • Aspergillus species

More on Farmer's Lung

Overview: Farmer's Lung
Differential Diagnoses & Workup: Farmer's Lung
Treatment & Medication: Farmer's Lung
Follow-up: Farmer's Lung
References
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References

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Further Reading

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Keywords

farmer's lung, farmer lung, farmer's lung disease, extrinsic allergic alveolitis, hypersensitivity pneumonitis, HP, wheezing, dyspnea, maple bark stripper's lung, chicken plucker's lung, bagassosis, byssinosis, humidifier lung, Actinomyces, Aspergillus, actinomycetes, Saccharopolyspora rectivirgula, S rectivirgula, Micropolyspora faeni, M faeni, Thermoactinomyces vulgaris, T vulgaris, Thermoactinomyces viridis, T viridis, Thermoactinomyces sacchari, T sacchari, Krebs von den Lungen-6, KL-6

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Contributor Information and Disclosures

Author

Laurianne G Wild, MD, FAAAAI, Acting Chief and Associate Professor of Clinical Medicine, Section of Clinical Immunology, Allergy and Rheumatology, Director, Allergy and Clinical Immunology Fellowship Training Program, Tulane University Health Sciences Center; Director, Allergy and Immunology Clinic, Veteran's Administration Medical Center at New Orleans
Laurianne G Wild, MD, FAAAAI is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, and Association of Subspecialty Professors
Disclosure: Nothing to disclose.

Coauthor(s)

Eduardo E Chang, MD, Fellow, Department of Allergy and Immunology, Tulane University
Disclosure: Nothing to disclose.

Medical Editor

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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